Fig. 2: Liver proteome remodeling due to hepatic lesions.
From: Noninvasive proteomic biomarkers for alcohol-related liver disease
a, Proteins in liver tissue that were significantly differentially abundant across stages of fibrosis, inflammatory activity and steatosis (FDR-corrected P < 0.05). n = 6/32/24/7/10 biologically independent samples for Kleiner score 0/1/2/3/4; n = 16/22/17/12/5/7 biological independent samples for NAS inflammation score 0/1/2/3/4/5; and n = 36/12/19/12 for NAS steatosis score 0/1/2/3. b, Hierarchical clustering of all significantly (sig.) dysregulated proteins in the liver proteome. Row clustering was based on median log2 intensity after z-score normalization across fibrosis stages F0–4. c, Fraction (%) of up- and downregulated liver-specific and secreted proteins. d, Top 20 proteins that correlate with Kleiner, NAS inflammation and NAS steatosis scores, respectively. Number of independent biological replicates for each disease group is the same as in a. e, Distribution of log2 intensity values of top four proteins correlating to each histologic score. The gray line in the middle of the box is the median, the top and bottom of the box represent the upper and lower quartile values of the data and the whiskers represent the upper and lower limits for consideration of outliers (Q3 + 1.5 × IQR, Q1 – 1.5 × IQR). IQR represents IQR (Q3 – Q1).
